抄録
Ionizing radiation induces DNA double-strand breaks, which result in cell death, if they are not repaired. Surviving cells repaired DNA damage, and they are expected to grow normaly, however, it is becoming clear that delayed reproductive death, delayed chromosomal aberrations, and delayed mutations are frequently observed in the progeny of surviving cells. These phenomenon called radiation-induced genomic instability in the progeny of surviving cells are studied extensively, but the mechanism underlying is not clear.We have hypothesized that DNA double-strand breaks may create potentially unstable chromosome regions (PUCR) at the broken sites through DNA double-strand break repair, and that PUCRs could be reactivated when chromatin structure is changed during DNA replication, or through gene expression. To prove the hypothesis, GM 638 cells (SV40-immortalized cells) are irradiated with 3 Gy of X rays, and the primary colonies having large deletions at the HPRT locus on X chromosome are isolated. The primary colonies are seeded again, and the frequency of colonies with giant cells were examined. We found that colonies with significant numbers of giant cells were detected about 7% among the secondary colonies. It is suggested that the secondary change may arise at PUCRs, and reactivated PUCRs could cause giant cells within the secondary colonies.
